Since the pioneering work of Hiatt and Bawol (1984), there has amassed a considerable amount of evidence that moderate-to-heavy alcohol consumption increases risk of breast cancer in women (Willettet al., 1987;Longnecker, 1999). A plausible mechanism is by alcohol's effects on circulating hormone levels. Alcohol administration has been reported to increase circulating oestradiol levels in pre-menopausal women (Reichman et al., 1993); the evidence is mixed in post-menopausal women (Purohit, 1998). In a cross-sectional study of pre-menopausal women, Muti et al.(1998) determined an association between reported alcohol consumption and serum oestradiol levels during the luteal phase of the menstrual cycle, and found an 18% elevation in drinkers, consuming an average 1 drink per day, compared to abstainers. It is not clear how alcohol affects circulating oestradiol levels. Alcohol has been reported to increase aromatase activity; i.e., the conversion of testosterone to oestrogens, resulting in reduced testosterone and increased oestrogen levels (Gavaler and Van Thiel, 1992). Alcohol also might interact with luteinizing hormone production from the pituitary (Rettori and McCann, 1997), resulting in increased oestradiol release from the ovaries.In addition to affecting oestrogen levels, alcohol appears to influence melatonin. Alcohol administration has been reported to reduce the nocturnal rise in serum melatonin in rats ( HYPERLINK "http://alcalc.oxfordjournals.org/content/36/3/276.long" \l "ref-14"Moss et al., 1986), and in humans ( HYPERLINK "http://alcalc.oxfordjournals.org/content/36/3/276.long" \l "ref-6"Ekman et al., 1993; HYPERLINK "http://alcalc.oxfordjournals.org/content/36/3/276.long" \l "ref-21"Rojmark et al., 1993) under experimental conditions.